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PRINCIPLES OF SURGERY November 2011 FLUID AND ELECTROLYTE BALANCE PART 2: DISORDERS OF ACID-BASE AND POTASSIUM BALANCE Dr. Bob Richardson Toronto General Hospital Objectives (1) Normal acid-base physiology Acid from diet Renal response to acid Pathophysiology of acid-base balance Effects of vomiting, bile, pancreatic fluid, ileostomy losses on acid-base balance Effect of kidney disease on acid base balance Metabolic acidosis from excess acid generation Metabolic alkalosis from vomiting Objectives (2) Therapy of metabolic acidosis Why, when, how much bicarbonate Normal Potassium homeostasis Hyper- and hypokalemia causes, manifestations emergency treatment Normal Acid-Base Physiology Input On a usual North American diet, acid is generated from metabolism of sulfurcontaining amino acids to sulfuric acid: methionine , cysteine H2SO4 Typical NA diet generates 50-100 mmol H+ daily Normal Acid-Base Physiology Buffering H+ added to body water must be buffered: Without buffering, one day’s protein intake would decrease blood pH to 3! Main buffer is bicarbonate: H+ + HCO3- H2CO3 CO2 + H2O Buffering greatly reduces the [pH] Buffering would gradually reduce ECF [HCO3] if new bicarbonate were not generated Normal Acid-Base Physiology Kidney Generation of New HCO3 In order to restore ECF bicarbonate lost to buffering, the kidney excretes acid in the form of ammonium (NH4+) made from glutamine Ammonium excretion increases with metabolic acidosis and respiratory acidosis in response to the decrease in cell pH Urine NH4+ can increase from 40 200 mmol/d with acidemia DIETARY PROTEIN 70 mmol H+ (+ SO4) - 70 mmol HCO3 + 70 mmol HCO3 KIDNEY URINE NET ACID (NH4+) 70 mmol Corollaries of Normal Physiology Low protein diets generate very little acid If kidneys fail, acidosis is inevitable If kidneys are healthy, chronic acid gain (e.g. diarrhea) may cause no acidosis If kidneys are not healthy, chronic acid gain (diarrhea) may cause severe acidosis Acid-Base Impact of Loss of GI Secretions Gastric 0.5-2 L/d 100 mM H+ Bile 1 L/d HCO3 40 mM Pancreas 2 L/d HCO3 70-120 mM Ileostomy 0.5-1 L/d HCO3 30 mM Colostomy 1 L/d HCO3 20 mM Diarrhea 1-20 L/d HCO3 up to 75 mM Alkalosis Acidosis Acidosis Acidosis Acidosis Acidosis Causes of Metabolic Acidosis Loss of HCO3-containing GI fluid (see table) Loss of HCO3 in urine: proximal RTA ( rare !) Kidney failure (GFR< 30 ml/min) Acid gain Lactic acidosis Ketoacidosis Methanol poisoning (formic acid) Ethylene glycol poisoning (a variety of organic acids) Salicylate poisoning The Anion Gap Acid gain results in an increase in the anion gap: Na – (Cl + HCO3) Consider lactic acidosis with gain of 10 mmol/L H+ and lactateBefore: Na 140 After:Na 140 Cl 102 Cl 102 HCO3 AG 25 13 HCO3 15 23 Significance of the Anion Gap Anion gap > 15 indicates accumulation of an organic acid anion in plasma Almost always means metabolic acidosis 5 conditions that cause acid gain with increased anion gap are potentially fatal and must be recognized Differential Dg of Metabolic Acidosis by Anion Gap Normal AG Diarrhea or other GI loss Kidney failure Renal tubular acidosis “Expansion” acidosis Increased Anion Gap Lactic acidosis Ketoacidosis Methanol poisoning Ethylene glycol poisoning ASA poisoning Case History: 70 year old woman on hemodialysis for 5 years. Presents with 6 hour history of cold left leg. One month earlier her BP was 150/80, Hgb 105 g/L, HCO3 20 mmol/L. For several weeks she has had abdo pain with bloody diarrhea. For one week she has been weak and dizzy and a little confused. On exam: confused, restless; atrial fibrillation @ 120/min BP 110/70; JVP low; mild abdominal tenderness. Left leg cool and pulseless below knee. Lab Values Hgb 60 g/L WBC 15 pH PCO2 PO2 HCO3 7.22 25 90 10 Na K Cl AST 140 5.5 103 300 Diagnosis Lactic acidosis Anemia Hypotension (atrial fib) Ischemic leg Ischemic bowel/liver Therapy of Metabolic Acidosis Metabolic acidosis is more important for diagnosis than therapy No trials proving bicarbonate therapy alters outcome Generally try and maintain pH > 7.00 and bicarbonate > 8 mmol/L Amount needed = [HCO3] X BWt (assuming severe acidosis) Metabolic Alkalosis from vomiting or gastric suction Bicarbonate generation: Loss of HCl from stomach Volume depletion (concentration) Renal bicarbonate retention Hypokalemia (from urine loss of K+ with bicarbonaturia and high aldosterone) Increased angiotensin II – stimulates proximal bicarbonate reabsorption How to Prevent Metabolic Alkalosis in a Patient on Gastric Suction Prevent volume depletion Prevent hypokalemia Replace gastric losses with normal saline Replace KCl Prevent HCl secretion Use PPI or H2 blocker Potassium Normal potassium homeostasis Hyperkalemia shift into and out of cells kidney regulation of potassium excretion cardiac effects cell shift impaired K+ excretion Hypokalemia cell shifts urine and GI losses Normal Potassium Distribution ICF K=140 mM ECF Na+ K+ K=4 mM Normal Potassium Balance ECF [K] 4 mM ICF 140 mM 2% in ECF 98% in ICF Daily intake 30-80 mmol (fruits, veggies) Note: one large K+ meal = total ECF K+ insulin promotes K+ uptake by cells P[K+] stimulates aldosterone Aldosterone stimulates K+ secretion and excretion K+ Shift K+ shift into cells insulin catecholamines (2 receptor) - e.g. ventolin anabolic state (growth, refeeding etc) K+ shift out of cells insulin deficiency - diabetes, fasting cell ischemia, necrosis (e.g. rhabdomyolysis), red cell lysis etc. K+ Excretion by Kidney Regulated at cortical collecting duct Aldosterone stimulates Na+ reabsorption Makes lumen negatively charged Negative charge attracts K+ from cell Flow rate also very important (volume) since excretion = concentration X flow Flow depends on GFR, volume state Major Factors Affecting K excretion Aldosterone Flow Hyperkalemia Cardiac Effects Life-threatening arrhythmias when P[K+] > 7 mM Abnormal ECG when P[K+] > 6.0 peaked T waves broad QRS flat P waves sine wave ECG ECG post acute treatment ECG post dialysis Hyperkalemia - Role of Kidney ALWAYS impaired K+ excretion as cause of hyperkalemia - usually both: Low flow to CCD: advanced renal failure severe ECF volume depletion oliguria, anuria Low aldosterone activity adrenal insufficiency (mineralocorticoid) impaired renin secretion or AII generation Drugs Promoting Hyperkalemia Block aldosterone generation by angII Block aldosterone action on CCD ACE inhibitors, angiotensin receptor blockers spironolactone amiloride, triamterene high dose Septra Multiple effects cyclosporine Case of Hyperkalemia 40 year old construction worker falls three stories from scaffold Multiple fractures - femur, ribs, humerus Compartment syndrome in thigh, calf Hypovolemic shock Serum potassium 5.2 6.5 over 2 hours Urine flow 10 ml/h CK 12,000 Diagnosis Shift of K out of cells Rhabdomyolysis Reduced renal excretion Very low CCD flow Hypotensive shock – reduced GFR, increased proximal reabsorption Oliguric ATN Management of Hyperkalemia Urgent: for P[K+]>7, arrhythmia or ECG changes: 1 amp calcium gluconate bolus 20 units insulin bolus (+ 1 amp 50% D/W) 2-4 puffs of ventolin or ventolin inhalation Semi-urgent increase urine flow - saline if appropriate furosemide hemodialysis Hypokalemia- Effects Cardiac: VPB’s, u-waves, VF and VT if cardiac ischemia Muscle weakness Metabolic alkalosis Impaired insulin secretion Hypokalemia - causes Shift into cells insulin high catecholamines - endogenous or exog. Increased loss GI - diarrhea, vomiting, fistulas, ostomies Urine: diuretics polyuria primary aldosteronism Treatment of Hypokalemia Oral KCl - 8 or 20 mmol/tablet or liquid IV KCl if urgent or unable to take orally 40 mmol/L max concentration, 40 mmol/h maximum rate most hypokalemic patients have high losses and volume depletion in monitored setting and central line can give boluses of 40/100 mL if volume a concern Potassium and IV Fluids Most hospitals committed to removing KCl from wards Prefer standard IV fluids with added KCl Usually 10 or 20 mmol/L High concentrations (20 mmol/100 ml) only in monitored setting using pumps and central lines